Evidence map›Paper›PMID 22140050›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries.

Lydia W M Nausch, Adrian D Bonev, Thomas J Heppner, Yvonne Tallini, Michael I Kotlikoff, Mark T Nelson

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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  6. Review
  7. Article
  8. Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Small-world connectivity dictates collective endothelial cell signaling.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Lydia W M NauschDepartment of Pharmacology, University of Vermont College of Medicine, Burlington, VT05405, USA. Mark.Nelson@uvm.edu
Adrian D Bonev
Thomas J Heppner
Yvonne Tallini
Michael I Kotlikoff
Mark T Nelson
University of Vermont · USNew York State College of Veterinary Medicine · US

Funding

Impact of SAH on Parenchymal Arterioles and Neurovascular CouplingP01HL095488 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BONEV, ADRIAN · 2010 to 2014
$11.4M
REGULATION OF CEREBRAL ARTERY DILATIONR01HL044455 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NELSON, MARK T · 1991 to 2010
$3.9M
NHLBI NIH HHS P01-HL-095488-01NHLBI NIH HHS R01-HL-44455
6 · The paper itself

Abstract

It is generally accepted that the endothelium regulates vascular tone independent of the activity of the sympathetic nervous system. Here, we tested the hypothesis that the activation of sympathetic nerves engages the endothelium to oppose vasoconstriction. Local inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) signals ("pulsars") in or near endothelial projections to vascular smooth muscle (VSM) were measured in an en face mouse mesenteric artery preparation. Electrical field stimulation of sympathetic nerves induced an increase in endothelial cell (EC) Ca(2+) pulsars, recruiting new pulsar sites without affecting activity at existing sites. This increase in Ca(2+) pulsars was blocked by bath application of the α-adrenergic receptor antagonist prazosin or by TTX but was unaffected by directly picospritzing the α-adrenergic receptor agonist phenylephrine onto the vascular endothelium, indicating that nerve-derived norepinephrine acted through α-adrenergic receptors on smooth muscle cells. Moreover, EC Ca(2+) signaling was not blocked by inhibitors of purinergic receptors, ryanodine receptors, or voltage-dependent Ca(2+) channels, suggesting a role for IP(3), rather than Ca(2+), in VSM-to-endothelium communication. Block of intermediate-conductance Ca(2+)-sensitive K(+) channels, which have been shown to colocalize with IP(3) receptors in endothelial projections to VSM, enhanced nerve-evoked constriction. Collectively, our results support the concept of a transcellular negative feedback module whereby sympathetic nerve stimulation elevates EC Ca(2+) signals to oppose vasoconstriction.

Indexed as

AnimalsCalciumCalcium SignalingConnexinsEndothelium, VascularFeedback, PhysiologicalGap Junction alpha-5 ProteinInositol 1,4,5-Trisphosphate ReceptorsIntermediate-Conductance Calcium-Activated Potassium ChannelsMesenteric ArteriesMiceMice, Inbred C57BLMice, TransgenicMuscle, Smooth, VascularReceptors, Adrenergic, alphaSympathetic Nervous SystemCalciumConnexinsGap Junction alpha-5 ProteinInositol 1,4,5-Trisphosphate ReceptorsIntermediate-Conductance Calcium-Activated Potassium ChannelsItpr1 protein, mouseReceptors, Adrenergic, alpha

Identifiers

PMID22140050
PMCPMC3353782
OpenAlexW2153542713

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.